FAM98A promotes proliferation of non-small cell lung cancer cells via the P38-ATF2 signaling pathway

Zheng, Rui; Liu, Quanbo; Wang, Tianxu; Wang, Lili; Zhang, Yong

doi:10.2147/cmar.s163323

Cited by 11 publications

(11 citation statements)

References 26 publications

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“…Our study showed that overexpression of C14orf159 could inhibit the phosphorylation of ERK and its direct downstream factor P90RSK. These results were similar to those of previous studies,5,15 which suggested that C14orf159 may abrogate gastric cancer cells’ invasion and proliferation by inactivating ERK signaling. A previous study showed that ERK inhibitor U0126 could inhibit the levels of p-ERK and Snail and then restore E-cadherin expression.…”

Section: Discussionsupporting

confidence: 92%

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<p>C14orf159 suppresses gastric cancer cells’ invasion and proliferation by inactivating ERK signaling</p>

Zhu¹,

Li²,

Gao³

et al. 2019

CMAR

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Background C14orf159, a new protein, has been identified recently. But its expression in tissues and clinicopathologic correlation is still unknown. Patients and methods We carried out immunohistochemistry staining in 144 gastric cancer cases in this study. Then Western blot was used to detect the expression of protein. MTT and matrigel invasion assay were used to assess the biological effects. Results The immunohistochemical results indicated that the expression of C14orf159 in normal gastric mucosa close to cancer tissue was remarkably higher than that in stomach carcinoma samples (63.9% and 34.7%, respectively, P <0.001). Negative C14orf159 expression was dramatically related to high TNM stages ( P =0.033) and positive lymph node metastasis ( P =0.008). Once C14orf159 was overexpressed, the expression levels of phosphorylated ERK and its regulated downstream molecules, such as Snail, phosphorylated P90RSK and Cyclin D1, were decreased, while the expression level of E-cadherin was increased. Finally, the invasion and proliferation capacity of gastric cancer cells was inhibited. Conclusion In other words, loss of C14orf159 is associated with the progression of gastric cancer. The role of C14orf159 in repression of proliferation and invasion may be due to resuming E-cadherin and abolishing Snail and Cyclin D1 expression through inactivating ERK–P90RSK pathway.

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Section: Discussionsupporting

confidence: 92%

“…To assess the sections, semi-quantitative scoring method was used by two pathologists with extensive diagnostic experience, but they were blinded to the clinical information. Staining intensity and percentage of stained cells were considered as described previously 5. A score ≥4 was regarded as positive C14orf159 expression.…”

Section: Methodsmentioning

confidence: 99%

<p>C14orf159 suppresses gastric cancer cells’ invasion and proliferation by inactivating ERK signaling</p>

Zhu¹,

Li²,

Gao³

et al. 2019

CMAR

Self Cite

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“…In NSCLC, high ATF2 levels were significantly associated with worse prognosis (146) and, recently, Zhou et al demonstrated that overexpression of ARHGEF39 led to increased ATF2 levels by activating the Rac1-p38-ATF2 signalling pathway promoting tumour invasion and proliferation (147). Similarly, Zheng et al showed that ATF2 activation triggers cell proliferation and lymph node metastasis in NSCLC (148). In extramammary Paget’s disease (EMPD), a rare malignancy of the skin, it was shown that p-ATF2 and p-STAT3 are both overexpressed and associated with the tumour stage: both markers displayed the highest expression levels in advanced EMPD (149).…”

Section: Introductionmentioning

confidence: 94%

The activating transcription factor 2: an influencer of cancer progression

Huebner

Procházka

et al. 2019

Mutagenesis

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In contrast to the continuous increase in survival rates for many cancer entities, colorectal cancer (CRC) and pancreatic cancer are predicted to be ranked among the top 3 cancer-related deaths in the European Union by 2025. Especially, fighting metastasis still constitutes an obstacle to be overcome in CRC and pancreatic cancer. As described by Fearon and Vogelstein, the development of CRC is based on sequential mutations leading to the activation of proto-oncogenes and the inactivation of tumour suppressor genes. In pancreatic cancer, genetic alterations also attribute to tumour development and progression. Recent findings have identified new potentially important transcription factors in CRC, among those the activating transcription factor 2 (ATF2). ATF2 is a basic leucine zipper protein and is involved in physiological and developmental processes, as well as in tumorigenesis. The mutation burden of ATF2 in CRC and pancreatic cancer is rather negligible; however, previous studies in other tumours indicated that ATF2 expression level and subcellular localisation impact tumour progression and patient prognosis. In a tissue- and stimulus-dependent manner, ATF2 is activated by upstream kinases, dimerises and induces target gene expression. Dependent on its dimerisation partner, ATF2 homodimers or heterodimers bind to cAMP-response elements or activator protein 1 consensus motifs. Pioneering work has been performed in melanoma in which the dual role of ATF2 is best understood. Even though there is increasing interest in ATF2 recently, only little is known about its involvement in CRC and pancreatic cancer. In this review, we summarise the current understanding of the underestimated ‘cancer gene chameleon’ ATF2 in apoptosis, epithelial-to-mesenchymal transition and microRNA regulation and highlight its functions in CRC and pancreatic cancer. We further provide a novel ATF2 3D structure with key phosphorylation sites and an updated overview of all so-far available mouse models to study ATF2 in vivo.

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“…Several studies have reported that the abnormal expression of family with sequence similarity 98 member A (FAM98A) is associated with multiple types of cancer, including ovarian, endometrial, colorectal and lung cancer ( 14 – 17 ). Akter et al ( 14 ) revealed that FAM98A, which is arginine-methylated by protein arginine methyltransferase 1 (PRMT1), was highly expressed in ovarian cancer cell lines, and found that the knockdown of FAM98A reduced ovarian cancer cell migration, invasion and colony formation.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, another study identified an association between the presence of FAM98A and advanced lung cancer. FAM98A was shown to act as an oncogene by activating the P38/activating transcription factor 2 signaling pathway to promote lung cancer cell proliferation and colony formation ( 17 ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑26a inhibits cell proliferation and invasion by targeting FAM98A in breast cancer

et al. 2021

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MicroRNAs (miRNAs/miRs) play key roles in cancer progression. Extensive research has revealed that miR-26a is abnormally expressed and functions as a tumor suppressor in numerous types of cancer. Thus, the present study was undertaken to investigate the regulatory role and potential mechanism of action of miR-26a in breast cancer. Furthermore, the present study aimed to examine the alterations in miR-26a expression and its effects on human breast cancer cells. Reverse transcription-quantitative PCR was conducted to assess the differences in miR-26a expression between human breast cancer and normal breast specimens. A Cell Counting Kit-8 assay and cloning experiments were used to detect cell proliferation and clone formation. Wound healing and Transwell assays were performed to examine cell migration and invasion. A luciferase activity experiment was utilized to validate the association between miR-26a and family with sequence similarity 98 member A (FAM98A). Western blotting was conducted to detect the protein expression levels of FAM98A, sonic hedgehog signaling molecule (SHH), smoothened, frizzled class receptor (SMO) and GLI family zinc finger 1 (GLI1). The results indicated that miR-26a expression was decreased in breast carcinoma tissues and cell lines. Moreover, overexpression of miR-26a significantly suppressed cell proliferation, clone formation ability and metastasis, and it sensitized breast cancer cells to docetaxel. It was demonstrated that miR-26a directly targeted FAM98A, and that FAM98A, SHH, SMO and GLI1 expression levels were decreased in cells transfected with miR-26a mimics. Collectively, the results of the present study suggested that miR-26a negatively regulated the expression of FAM98A, indicating that it may play a key role in the suppression of breast carcinogenesis.

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FAM98A promotes proliferation of non-small cell lung cancer cells via the P38-ATF2 signaling pathway

Cited by 11 publications

References 26 publications

<p>C14orf159 suppresses gastric cancer cells’ invasion and proliferation by inactivating ERK signaling</p>

<p>C14orf159 suppresses gastric cancer cells’ invasion and proliferation by inactivating ERK signaling</p>

The activating transcription factor 2: an influencer of cancer progression

MicroRNA‑26a inhibits cell proliferation and invasion by targeting FAM98A in breast cancer

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FAM98A promotes proliferation of non-small cell lung cancer cells via the P38-ATF2 signaling pathway

Cited by 11 publications

References 26 publications

<p>C14orf159 suppresses gastric cancer cells&rsquo; invasion and proliferation by inactivating ERK signaling</p>

<p>C14orf159 suppresses gastric cancer cells&rsquo; invasion and proliferation by inactivating ERK signaling</p>

The activating transcription factor 2: an influencer of cancer progression

MicroRNA‑26a inhibits cell proliferation and invasion by targeting FAM98A in breast cancer

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Product

Resources

About

<p>C14orf159 suppresses gastric cancer cells’ invasion and proliferation by inactivating ERK signaling</p>

<p>C14orf159 suppresses gastric cancer cells’ invasion and proliferation by inactivating ERK signaling</p>